Studies performed during the initial funding period revealed that F(ab')2 fragments of immmune IgG were completely ineffective in suppressing the neonatal burst of ecotropic virus and, subsequently, had no leukemosuppressive activity. Since these preparations retained full neutralizing activity, the results suggest that prevention of neonatal virus expression by immune IgG occurs via a mechanism other than simple virus neutralization. Therapy initiated beyond day 4 of life, no matter how extensive, failed to eliminate ecotropic virus infectious cell centers (ICC). Identical results were obtained when combined anti-gp71 antibody plus complement therapy was attempted. Using our standard therapy protocols, it was found that anti-p15E, either alone or in combination with complement, was incapable of suppressing early tissue ICC or eventual leukemia development. Attempts to characterize the virus-expressing subpopulations in AKR tissues have revealed that within the first 4 weeks of life thymic ICC are contained solely in the cortisone sensitive population of immature, cortical thymocytes. With increasing age, ICC gradually shift into the more mature medullary population. Parallel experiments using peanut agglutinin (PNA) confirmed these findings, revealing ICC solely in the PNA+ thymocyte population, eventually becoming equally distributed in PNA+ and PNA- populations. Treated AKR mice have also been analyzed for their antiviral antibody responses. Well over 85% of treated mice develop anti-gp71 antibody titers. These antibodies do not appear until 3 to 4 months of age, long after the early suppression and partial return of ICC activity in treated mice. (IT)